A cut gives pain; a toothache is a pain. The death of one we love causes us pain.
THEORIES OF PAIN.
1. Pre-renaissance. Theories of pain date to ancient civilizations where pain was thought to be inflicted by gods or due to imbalance in 'vital energies' or 'body humors'. At this time, Aristotle proposed that the heart was the centre of sensation, and thus pain was an affective quality. Hippocrates, however, viewed the brain as the centre of sensation. Descartes, in the early 17th century described nerves as tubes containing threads, each connecting an area of skin directly to the brain, the seat of sensation.
2. Early science. By the late 19th century, two distinct pain theories had emerged. The 1st proposed that pain is a specific sensation served by dedicated nerves independent of other sensations, the 'specificity theory'. A 2nd pain theory, the 'summation theory', was proposed suggesting that pain was the product of any sensory modality given a stimulus of sufficient intensity. The earlier view of pain as an affective quality remained until a new theory of pain emerged in the 1950s. This 'sensory interaction theory' incorporated two components: the sensation of pain (dependent on physiological processes) and the reaction to it (dependent on cognitive and affective processes). This theory proposed the involvement of two systems in pain transmission. One consisted of slowly conducting small fibres whose activation produced painful sensations. The other consisted of faster-conducting larger fibres whose activation inhibited transmission of small fibre impulses in the dorsal horn.
3. Gate- control theory. This was effectively a synthesis of the strongest elements of all these main theories.It recognized the specificity of peripheral pain systems, central summation, and input modulation via larger sensory fibres and psychological influences. The gate- control theory proposed a spinal gating mechanism in the dorsal horn that was influenced by the relative amounts of activity in large and small fibres and by descending controls from the brain. Thus, pain is a complex experience of somatic mechanisms and psychological influences ( affective and cognitive) and, as such, is always subjective in nature.
4. Current model. Increasing neuroscience evidence suggests that the nervous system is capable of substantial plasticity. This is the ordered alteration of structure or function due to development, experience, or injury. Central neurons have the capacity to change their responsiveness in spatial, temporal, and amplitude aspects to a given stimulus, especially if the stimulus is chronic. This 'jungle of neurochemical anatomy' can undoubtedly account for this plastic nature but the exact mechanisms are still being elucidated. The plasticity theory is the most comprehensive pain model to date.
CLASSIFICATION OF PAIN: physiological or pathological? The pain is either physiological (normal) or pathological (abnormal), although there is no universally accepted system. Physiological pain results from the activation of peripheral nociceptive afferents by noxious (potentially harmful) stimuli assuming baseline sensitivity of the sensory system and serves to warn of impending tissue injury. Here, pain is a normal experience that is essential to the survival of the individual. Pathological pain is distinguished by a change in baseline sensitivity of the nervous system and occurs after injury. This serves to protect the individual from further injury while healing occurs, an adaptive response. Pathological pain is termed 'maladaptive' when the sensitivity of the sensory system does not return to normal after tissue healing. Nociceptive pain is pain that occurs due to normal activation of the nociceptive system either by impending tissues injury or ongoing tissue destruction or inflammation. (Neuropathic Pain, Dr. Michael Bennett, Oxford, 2007)